Search PubMed⌕ Search

Biomedical subjects

P Reiss

Publications and source records attributed to P Reiss.

At least 109 records · Page 6Linked to original sources
PubMed1991

Clinical significance of small-intestinal microsporidiosis in HIV-1-infected individuals.

To assess the importance of microsporidiosis of the small intestine in the pathogenesis of chronic diarrhoea in HIV-1-infected individuals, duodenal biopsy samples from the following three patient groups were prospectively evaluated for bacterial, viral, and parasitic pathogens by standard methods, and for microsporidia by light microscopy: 55 consecutive HIV-1-antibody-positive subjects with unexplained diarrhoea of at least 3 weeks duration (group A); 38 HIV-1-seropositive subjects without diarrhoea (group B) who consecutively underwent upper gastrointestinal endoscopy for various reasons; and 7 patients without known risk factors for HIV infection with chronic unexplained diarrhoea (group C). In groups A and B most subjects had had previous AIDS-defining opportunistic infections and the median peripheral blood CD4 lymphocyte count was less than 0.1 x 10(9)/l. Microsporidia were detected as the single pathogen in 15 of the group A compared with 1 (in whom diarrhoea subsequently developed) of the group B patients (p = 0.001) and none of the group C patients. With the exception of 4 of the group A patients, no other intestinal pathogens were identified in any of the patients. The median peripheral blood CD4 count was significantly lower in patients with detectable microsporidia than in those without microsporidiosis (0.03 x 10(9)/l vs 0.06 x 10(9)/l; p = 0.03); in all patients with microsporidiosis, the CD4 count was equal to or less than 0.1 x 10(9)/l. 13 patients with microsporidiosis were treated with metronidazole, in 10 of whom treatment led to a substantial improvement or disappearance of diarrhoea within days of starting therapy, but did not result in eradication of the parasite in the 5 patients who underwent repeat biopsy. The findings suggest that small-intestinal microsporidiosis is an important cause of chronic unexplained diarrhoea in HIV-1-infected individuals with pronounced cellular immune deficiency. This infection should therefore be added to the list of AIDS-defining opportunistic infections.

Acquired Immunodeficiency Syndrome↗
PubMed1991

[Pneumocystis carinii infection during prophylaxis with nebulized pentamidine in a patient with AIDS].

Since the introduction of aerosolised pentamidine for prophylaxis against Pneumocystis carinii pneumonia (PCP) in HIV-seropositive persons and patients with AIDS, an increasing number of cases of atypical manifestations of infection with Pneumocystis carinii have been reported in the United States, viz. upper lobe pneumonia, extrapulmonary Pneumocystis carinii infection and spontaneous pneumothorax. An association between these atypical manifestations of Pneumocystis carinii infection and the use of aerosolised pentamidine seems likely. This report is the first description in the Netherlands of an atypical Pneumocystis carinii infection in an AIDS patient while using aerosolised pentamidine for prophylaxis against PCP. Since aerosolised pentamidine for prophylaxis against PCP is increasingly being used in the Netherlands, a rise in incidence of atypical manifestations of Pneumocystis carinii infection can be expected.

Acquired Immunodeficiency Syndrome↗
PubMed1991

Contribution of antibody response to recombinant HIV-1 gene-encoded products nef, rev, tat, and protease in predicting development of AIDS in HIV-1-infected individuals.

The relation between antibody-response profiles to Escherichia coli-produced HIV-1 nef, rev, tat, and protease proteins and the risk of developing AIDS was studied using stored serum samples taken sequentially from a cohort of 195 initially symptom-free men who were seropositive for antibodies to HIV-1 structural proteins and 72 men who seroconverted for such antibodies. The AIDS attack rates at 39 months follow-up were significantly higher in the men with negative versus positive antibody profiles to nef, tat, and protease, respectively. [Difference (D) between attack rates = 11.279, 5.884, and 8.322, respectively]. No significant difference was found between men with negative versus positive antibody profiles to rev. The above differences between AIDS attack rates were clearly lower than those reported from the same cohort for men who were serum HIV-1 antigen positive versus negative, and for men with low versus normal CD4+ lymphocyte counts, but with respect to nef antibody-response profiles, resembled the difference reported between anti-HIV-1 core antibody-negative versus antibody-positive men. In the subgroup of men without any of the markers previously found to be predictive of progression to AIDS in the cohort (persistent HIV-1 p24 antigenemia, low anti-HIV-1 anti-core antibody reactivity, and low CD4+ cell counts), antibody profiles to nef, rev, tat, and protease did not contribute to the prediction of outcome of infection. When used in combination with persistent HIV-1 p24 antigenemia and low CD4+ cell counts, negative antibody profiles to nef and protease, respectively, were equally sensitive and specific in predicting progression to AIDS, as was low anti-HIV-1 anti-core antibody reactivity.

Acquired Immunodeficiency Syndrome↗
PubMed1990

[Zidovudine therapy in 141 patients with symptoms of HIV infection; a multicenter study].

We describe the results of treatment with zidovudine in 141 symptomatic HIV positive patients, 119 of whom had AIDS. Total mortality was 30% over a mean observation period of 45 weeks after the start of the treatment. This is much lower than the mortality among AIDS patients in the pre-zidovudine period. During the first 2 months the feeling of wellbeing and the body weight increased, but after 4 months these effects declined. Two months after start of therapy the number of new opportunistic infections declined, but it increased thereafter. Side effects were frequent: after 7 months zidovudine had to be reduced or even stopped in 43% of the patients mostly because of anaemia and/or leukopenia. After 6-7 months 45% of all patients had been given packed cells transfusions with a mean of 16 units. In general tolerability of zidovudine was better in patients with a higher number of circulating CD4-positive cells at the start. These results confirm that the effect of zidovudine in symptomatic HIV infected patients is favourable but only of limited duration.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Speed of progression to AIDS and degree of antibody response to accessory gene products of HIV-1.

Antibodies to E. coli-produced HIV-1 nef, rev, tat, vpu, and vpr proteins were measured by enzyme immunoassay in serial sets of sera from 72 men seroconverting for antibodies to HIV-1 structural proteins, and from 190 initially symptom-free men who were seropositive for these antibodies at entry into the study. In the men seroconverting for antibodies to structural proteins the levels of nef-, rev-, and tat-specific antibodies, but not of vpu-, and vpr-specific antibodies, within 3 months of seroconversion, appeared to be lower in the five men progressing to AIDS, compared with the men remaining symptom-free during follow-up. Analysis of the prevalence of previously described antibody profiles to these accessory gene products was carried out. In all HIV-1 antibody seroconverters and in those HIV-1 antibody seropositive men with 15 or more months of follow-up who progressed to AIDS, there was a shift from predominantly nef- and vpu-specific antibody negative profiles in the men developing AIDS in the early years of the study to predominantly nef- and vpu-specific antibody positive profiles in men who developed AIDS later. Rev- and tat-specific antibody negative profiles were dominant in men progressing to AIDS throughout follow-up. No vpr-specific antibody profile occurred preferentially in the men progressing to AIDS throughout follow-up. Low antibody reactivity to accessory gene products nef, rev, and tat appears, like low anti-core antibody reactivity, to be associated with progression to AIDS relatively rapidly after infection with HIV-1.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Temporary increase in serum beta 2-microglobulin during treatment with interferon-alpha for AIDS-associated Kaposi's sarcoma.

Beta 2-microglobulin (beta 2-M) levels were determined in the serum of 24 patients treated with high-dose human recombinant interferon-alpha (IFN alpha) for AIDS-associated Kaposi's sarcoma. There was a significant increase in serum beta 2-M levels, irrespective of the response to treatment. However, the increase of serum beta 2-M levels in responders appeared to be more pronounced than in those with progressive disease, but this difference was not significant. The increase was only found during the initial 8 weeks; thereafter, beta 2-M levels declined in patients with continuing clinical improvement during ongoing treatment with IFN alpha. This may have been related to IFN alpha dose modification at 8 weeks for all patients. The initial rise in serum beta 2-M might be related to the immunomodulation properties of IFN alpha. Because serum beta 2-M levels were also enhanced in non-responders, this rise does not demonstrate that immunomodulation by IFN alpha is a mechanism of anti-tumour activity in AIDS-associated Kaposi's sarcoma.

Acquired Immunodeficiency Syndrome↗
PubMed1990

HIV-1 P24 antigenaemia does not predict time of survival in AIDS patients.

The time of survival in 176 AIDS patients was investigated in relation to the presence or absence of HIV-1 p24 antigenaemia at the moment of diagnosis. The median time of survival in p24 antigen positive patients was 12 months, in p24 antigen negative patients it was 13 months; no difference in survival curves was found. Also no difference was found in survival between patients with high and low p24 antigen levels. The median time of survival in patients for whom a diagnosis of AIDS was made in the period before the introduction of zidovudine treatment was 10 months; in patients diagnosed in the period thereafter it was 18 months (p less than 0.005). However, when each period was analysed separately, no difference in survival between p24 antigen positive and negative patients was found. Separate analysis of patients with a diagnosis of Kaposi's sarcoma alone showed similar results. HIV-1 p24 antigenaemia at the moment of diagnosis of AIDS (both in the period before and in the period after the introduction of zidovudine) is not a predictor for time of survival.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Failure to maintain high-dose treatment regimens during long-term use of zidovudine in patients with symptomatic human immunodeficiency virus type 1 infection.

Long-term tolerance of zidovudine treatment was retrospectively analysed in 97 patients with AIDS or AIDS-related complex. After one year of treatment 68% and after two years 87% of the patients had had at least one dose adjustment during their course of therapy. Myelotoxicity was the most common cause (58% of all cases) of dose reductions and therapy interruptions (dose adjustments). At the time of the first dose adjustment 33 patients (34%) were suffering from anaemia (Hb less than 6.0 g/dl), 20 patients (21%) from leukopenia (leukocytes less than 1.5 x 10(9], and 10 patients (10%) from thrombocytopenia (thrombocytes less than 75 x 10(9]. Fifty-six patients (57%) needed one or more blood transfusions during therapy. The median time from the start of therapy to the time of the first dose adjustment was 14 (range: 2-64) weeks in patients who had a first dose adjustment because of anaemia without co-existing leukopenia or thrombocytopenia, and 37 (range: 6-85) weeks in patients who had a first dose adjustment because of leukopenia without co-existing anaemia or thrombocytopenia (p = 0.01). Peripheral blood CD4 positive lymphocyte counts less than or equal to 100/mm3, anaemia, and CDC classification IV-C1 at the start of treatment were associated with a need for an early dose modification or blood transfusion rather than the need for dose modification per se.

AIDS-Related Complex↗
PubMed1990

Antibody response to viral proteins U (vpu) and R (vpr) in HIV-1-infected individuals.

Antibodies to E. coli-produced HIV-1 vpr and vpu were determined by enzyme immunoassay in serial sets of sera from 72 men seroconverting for antibodies to HIV-1 structural proteins, and from 196 initially symptom-free men who were positive for such antibodies at study entry. First detection of vpr- and vpu-specific antibodies always was within 12 months of seroconversion for antibodies to structural proteins. In the combined cohort of 268 men, vpr- and vpu-specific antibodies were found persistently in 26 and 43% of men, respectively. Vpr- and vpu-specific antibodies were transiently detected in 3 and 7%, respectively, and intermittently detected in 18 and 13% of men, respectively. No association was found between the patterns of vpr- or vpu-specific antibody response and clinical outcome. In subjects with different patterns of vpr- and vpu-specific antibody response, no clear temporal relationship existed between the appearance or disappearance of antibodies and the onset of HIV-1-related disease.

Cross-Sectional Studies↗
PubMed1989

The serology and immunochemistry of HIV-induced platelet-bound immunoglobulin.

A study was carried out on the presence of platelet-bound immunoglobulins, platelet-bound complement and serum immunoglobulin reactive with platelets in the blood of persons infected with HIV and those at risk of HIV infection. Platelet-bound immunoglobulins, predominantly IgG and IgM, but not complement, were demonstrated by immunofluorescence in 16 out of 16 patients with AIDS, in 5 out of 7 with AIDS-related complex/persistent generalized lymphadenopathy and in 7 out of 10 apparently healthy sexually active homosexual men, of whom 2 were anti-HIV1 seropositive. There was no correlation between the presence of platelet-bound immunoglobulins and either the platelet count or the level of circulating immune complexes. The specificity of the platelet-bound immunoglobulins and platelet-reactive immunoglobulins in the corresponding sera was studied. Platelet-bound immunoglobulins were eluted and then investigated for cross-reactivity with HIV. Both sera and eluates were tested for reactivity with cardiolipin and reactivity with the major target antigen in classical autoimmune thrombocytopenia, the GP IIb/IIIa complex. Of 17 eluates containing platelet-reactive immunoglobulins, 5 reacted with HIV-determinants but 2 out of 5 eluates that did not contain platelet-reactive immunoglobulins also reacted. Although anti-cardiolipin antibodies were detected in all sera, none of the 17 eluates reacted with cardiolipin. Moreover, sera and eluates, reactive with normal platelets, did not react with type-1-Glanzmann disease platelets. This indicates that the antibodies are directed against the glycoprotein IIb/IIIa complex of platelets. This could not be confirmed by immunoprecipitation or by immunoblotting, however. We conclude that the presence of platelet-bound immunoglobulins is common in HIV-infection but may also occur in persons at risk and that the nature of the auto-antibodies is not different from that of the auto-antibodies observed in classical ITP.

AIDS-Related Complex↗
PubMed1989

Low antigenicity of HIV-1 rev: rev-specific antibody response of limited value as correlate of rev gene expression and disease progression.

An enzyme immunoassay based on an E. coli-produced HIV-1 rev gene product was used to detect rev-specific antibodies in longitudinally collected serum samples from 196 initially symptom-free men who were seropositive for antibodies to HIV-1 structural proteins and 72 men who seroconverted for such antibodies. In 61% of men no rev-specific antibodies were detected at all, 30% had persistently detectable rev-specific antibodies, and in 9% rev-specific antibodies were only transiently or intermittently detected. When a persistent rev-specific antibody response occurred in subjects who seroconverted to structural proteins, it was always, with one exception, found within 12 months of seroconversion. The rev-specific antibodies were also studied in a transectional sample of sera from the men who remained symptom-free and from those who developed AIDS-related conditions or AIDS, as well as in sera from 31 other men with AIDS-related conditions and in sera from 6 of these men at the time they developed AIDS. The rev-specific antibodies were found in 34% of symptom-free men, in 28% of patients with AIDS-related conditions, and in 16% of patients with AIDS. The low incidence of rev-specific antibodies early after infection may be due to low antigenicity of rev. The lower prevalence of rev-specific antibodies in sera from patients with AIDS, compared with patients with AIDS-related conditions and symptom-free HIV-1-infected individuals, may be explained by a progressive HIV-1-induced immunodeficiency.(ABSTRACT TRUNCATED AT 250 WORDS)

Acquired Immunodeficiency Syndrome↗